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TNF{alpha}-induced ATF3 expression is bidirectionally regulated by the JNK and ERK pathways in vascular endothelial cells

Koichi Inoue1,{dagger}, Takeru Zama1,3, Takahiro Kamimoto1, Ryoko Aoki1, Yasuo Ikeda3, Hiroshi Kimura2 and Masatoshi Hagiwara1,2,*

1 Department of Functional Genomics, Medical Research Institute, and 2 Laboratory of Gene Expression, School of Biomedical Science, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Janpan
3 Department of Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan

ATF3 (Activating transcription factor 3), a member of the CREB/ATF family, can be induced by stress and growth factors in mammalian cells, and is thought to play an important role in the cardiovascular system. However, little is currently known about how the induction of ATF3 is regulated, except that the JNK pathway is involved. Here, we investigated the differential roles of the MAPK pathways involved in TNF{alpha} (tumour necrosis factor {alpha})-induced ATF3 expression in vascular endothelial cells. In human umbilical vein endothelial cells, the expression of constitutively active MKK7 (MAPK kinase 7) increased the number of ATF3-positive cells, and dominant negative MKK7 suppressed the TNF{alpha}-induced expression of ATF3, indicating a requirement for the JNK pathway. In contrast, the expression of constitutively active or dominant negative MEK1/2 (MAPK/ERK kinase 1/2) suppressed or enhanced TNF{alpha}-mediated induction of ATF3, respectively. In support of this, the MEK1/2 specific inhibitor U0126 enhanced the expression of ATF3 induced by TNF{alpha}. Furthermore, the ERK pathway inhibits the TNF{alpha}-mediated induction of ATF3 mRNA, but not its stability, suggesting the involvement of ERK activity in the transcriptional regulation of the ATF3 gene. Our results suggest that TNF{alpha}-induced ATF3 gene expression is bidirectionally regulated by the JNK and ERK pathways in vascular endothelial cells.

Communicated by: Hiroshi Handa

{dagger}Present address: Department of Physiology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hamamatsu, Shizuoka 431-3192, Japan.

* Correspondence: E-mail: m.hagiwara.end{at}mri.tmd.ac.jp




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